Stomach and Duodenum 3 ppt - Aqeel Shakir Mahmood

Stomach and Duodenum

Dr Aqeel Shakir MahmoodAssistant ProfessorConsultant General and Laparoscopic SurgeonFICMS General SurgeryCABS General SurgeryFICMS-GIT Gastrointestinal Surgery (subspecialty )MRCS –( Ireland) General SurgeryFRCS –( London) General Surgery

Stomach and Duodenum

Anatomy Physiology Pathology Gastritis Peptic ulcer diseases Operative procedures Tumors Carcinoma of the stomach Other conditions

Tumours of the stomach and duodenum

INTRODUCTION - STOMACH
Benign Polyps Hyperplastic Fundic gland Neoplastic Multiple Tumors Leiomyomas Lipomas Heterotopic pancreas
Malignant Tumors Carcinoma Lymphoma Sarcoma Carcinoid Others Menetriers Disease Bezoar Volvulus

GASTRIC POLYPS

Hyperplastic polypsMost common type of polyp (65 – 90%)Inflammatory or regenerative polypsIn reaction to chronic inflammation or regenerative hyperplasiaSessile and seldom pedunculatedMostly in the antrumMultiple in 50% of casesVarying in size but seldom < 2cmRate of malignant transformation 1 – 3%Usually larger than 2 cm

GASTRIC POLYPS

Neoplastic polyps Types Tubular Villous (often larger - > 2cm - and malignant) Macroscopically More often in antrum Pedunculated with malignant potential Solitary, large and ulcerated Treatment Endoscopic removal if no malignancy identified with surveillance Excision with malignant focus or where endoscopic removal failed

GASTRIC POLYPS

Multiple gastric polypsRare conditionAdenomatous and hyperplastic polyps20% incidence of adenocarcinomaTreatmentIf confined to corpus and antrum – distal gastrectomyOtherwise total gastrectomySometimes associated with Polyposis syndromesFAPGardnerPeutz-JeghersCowdenCronkhite Canada

GASTRIC LEIOMYOMA

PathologyArise from smooth muscle of the GIT tractDifficult to distinguish from GIST75% benignDifferentiation only on mitotic indexLarge protruding with central ulcerUsually presents with bleeding Treatment is local excision with 2 – 3cm margin

GASTRIC LIPOMA

Rare submucus lesions Asymptomatic On routine endoscopy Require no treatment

GIST

Gastro intestinal stromal tumor

Role of Surgery in Primary Disease

Surgery is the principal treatment and the only curative therapy for localized, resectable primary disease

Surgical Treatment of primary GISTPearls for the Surgeon

GIST lesions are highly vascularized and have a fragile pseudocapsule Minimize the risk of tumor rupture GIST rarely involve regional nodes Lymphadenectomy not necessary The margins of resection from the tumor specimen should be carefully oriented and examined

Gastric GIST: Laparoscopic Approach

Gastric GIST

Inoperable Disease
6 Months after Imatinib

Gastric Cancer

Surgical anatomy

Introduction

The detection of gastric cancer in the early stage is vitally important in ensuring an excellent prognosis.

Early gastric cancer, whereby disease is limited to mucosa and submucosa, confers a 5 years survival rate of greater than 90% in many centers. when discovered in it 's symptomatic phase with a 5-year survival rate of less than 20%.

Introduction

The most recent estimation shows that gastric cancer is The Fourth most common cancer. The Second most common cause of cancer deaths worldwide.

Estimated cancer deaths. Ten most common sites,
percentagePercentage
Both sex
Female
Male Mmale ale
cancer
17.8
1103000
293000
810000
Lung
10.4
647000
241000
405000
Stomach
8.8
549000
165000
384000
liver
7.9
492000
238000
255000
colorectal
6.0
373000
373000
0
Breast
5.4
338000
111000
227000
Osophagus
4.7
233000
233000
0
Cervix uteri
3.4
213000
101000
112000
Pancreas
3.3
204000
0
204000
Prostate
3.1
195000
86000
109000
Leukemia

Introduction
The incidence of gastric cancer varies markedly in different areas of the world . The male preponderance of 2:1 is encountered world wide . the disease is rarely seen before the age of 40 years and the incidence varies sharply with age . The incidence and mortality is double for males in both high and low risk countries.

Introduction

Cancer of the stomach is three times more commom in social class 4 and 5 ( semiskilled, unskilled laborers ) than in social class 1 and 2 (professional , executive and higher manager )

ADENOCARCINOMA OF THE STOMACH

Symptoms and signs Vague discomfort difficult to distinguish from dyspepsia Anorexia Meat aversion Pronounced weight loss At late stage Epigastric mass Haematemesis usually coffee ground seldom severe Metastasis Vircho node in neck Blumer shelf in rectum

Classification of gastric carcinoma

several classifications of gastric carcinoma exist , like lauren ( finnish ) (D.I.O.)classification . Japanese classification (for early gastric cancer ) . Bormann classification (for advance gastric cancer).

lauren classification

This recognize two main groups with different histogenesis and aetiology . the first group is known as intestinal gastric cancer , as the gastric carcinoma cells exhibit a striated (brush) border and generally resembles intestinal cells , they tend to form localized expanding or ulcerating lesion and frequently surrounded by inteseinal metaplasia .

lauren classification

The second group is known as the diffuse gastric cancer as the lesion infiltrates the gastric wall without forming large disecrete masses , this carries worser prognosis than the intestinal type and arise from apparently normal gastric mucosa. Both the intestinal and diffuse cancers account for 90% of all gastric carcinoma , the remainder has a mixed morphology and are referred to as others

The Japanese classification
The Japanese Endoscopic Society has classified the macroscopic appearances of EGC into Type I protruded Type II superficial a-elevated, b-flat, c-depress Type III excavated

Bormann classification

Bormann classification of advance gastric cancer Type 1 polypoid Type 2 carcinomatous ulcer without invasion of adjacent mucosa Type 3 carcinomatous ulcer with invasion of adjacent mucosa Type 4 diffusely infiltrative linitis plastic

There were several staging for gastric cancer ,however an intermediate staging system has been the new TNM classification The important prognostic factors in patient without detectable distant metastasis are Depth of invasion of the gastric wall and LN spread, other significant variables are type of cancer(intestinal or diffuse) location of tumor (growth of cardia has poorer prognosis than middle or lower third) and the histological type(degree of differentiation

Staging of gastric cancer TNM

T—primary tumor T1 –tumor invasion of mucosa or mucasa and submucasaT2 - tumor invasion of muscularis propria or subserosaT3- tumor penetrating of serosaT4- tumor invasion of adjacent structures

N –regional lymph nodes N0- no evidence of LN metastasis N1- metastasis to group 1 LN Right paracardia LN Left paracardial LN Lesser curvature LN Greater curvature LN Suprapyloric LN Infrapyloric LN

N2--metastasis to group 2 LN

LN along the left gastric artery LN along the common hepatic artery LN along the celiac artery LN along the splenic hilum LN along the slenic artery

N3-- metastasis to group 3 LN

LN in the hepatoduedenal ligament LN in the retropancreatic head LN along the superior mesenteric vessels LN along the middle colic vessels Paraoartic LN LN in the anterior pancreatic head LN in the inferior pancreas Infradiaphragmatic LN LN in the esophageal hiatus of the diaphragm

M – distant metastasis Mo - no evidence of distant metastasis M1- evidence of distant metastasis

Etiological Factors

Gastric carcinogenesis is a multifactorial process. Following the classical epidemiological model, it represents the interaction of three major sets of factors: The agent (Helicobacter pylori). The host. The external environment.

The target tissue for this interaction is the gastric mucosa .

Screening
In high-incidence areas: asymptomatic groups In low-incidence areas: symptomatic groups Dyspeptic patients . Patients on Acid suppression therapy. Patients with Helicobacter pylori infection. Premalignant lesions/conditions.

Screening in low-incidence areas:symptomatic groups

Dyspeptic patients Dyspeptic symptoms are common in patients with EGC. It has been suggested that 60–90% of patients with EGC have dyspeptic symptoms ,as defined by the presence of heartburn or abdominal pain or discomfort centered in the upper abdomen. These symptoms are generally identical to those with benign gastric disease. Gastroscopy is seen as an approach to influence the stage of cancer at diagnosis.

Screening in low-incidence areas:symptomatic groups

2 . Patients on Acid suppression therapy The symptoms of EGC are often can not be differentiated from those of benign disease. This group of patients may be started on treatment with acid suppression drugs, including proton pump inhibitors and H2 blockers before referral to a specialist or before gastroscopy. The diagnosis of EGC can potentially be delayed as a result of an improvement in dyspeptic symptoms.

Screening in low-incidence areas:symptomatic groups

Patients on Acid suppression therapy EGC may also ‘heal’ by acid suppression, and make endoscopic identification of the EGC impossible, even by experienced endoscopists. ‘Healing’ of a malignant ulcer has been observed within 4 weeks with proton pump inhibitors

Screening in low-incidence areas:symptomatic groups

Patients on Acid suppression therapy

However, 37% of patients with gastric cancer, who were previously taking acid suppression therapy, were missed at index gastroscopy. This led to a mean delay in diagnosis .

Patients on Acid suppression therapy

Primary care physicians should therefore refrain from prescribing acid suppression drugs in patients over the age of 45 years with dyspepsia before endoscopy in order to minimize the risk of missing EGC. primary care physicians should be educated on the fact that the majority of patients with EGC have dyspeptic symptoms.

Screening in low-incidence areas:symptomatic groups

3. Patients with Helicobacter pylori infectionThere is compelling evidence for the role of H. pylori in the initiation of Correa’s cascade (stepwise progression from Chronic Active Gastritis, Atrophic Gastritis, Intestinal Metaplasia, Dysplasia and finally Carcinoma insitu and than Adenocarcinoma).

Helicobacter pylori

Gram-negative Microaerophilic Inhabits various areas of the stomach and duodenum. First discovered in 1983 by Dr Barry J. Marshall and Dr J. Robin Warren. Marshall and Warren were awarded the 2005 Nobel Prize for Medicine & Physiology.

Helicobacter pylori infection and gastrointestinal diseases

There is significant correlation between Helicobacter pylori infection and duodenal/gastric ulcer and gastric malignancy
Gastric ulcers ca 70 – 90 % Gastric cancers ca 60 – 90 % H. pylori colonies
Duodenal ulcers ca 95 %

Helicobacter pylori

Several epidemiological studies have also indicate that populations with H. pylori infection are at increase risk of developing gastric cancer.

Helicobacter pylori

There are emerging data that intestinal metaplasia and atrophic gastritis regress after H. pylori eradication. So H. pylori screening and treatment is an effective strategy in cancer prevention

Diagnosis of H. pylori

Invasive Tests
Gastroscopy Rapid Urease Test (RUT) Histology Culture Serology Antibody Test PCR
Non-invasive Tests
Urea Breath Test (UBT) 13C & 14C Antigen Test (Stool) Urine Test
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Urea Breath Test

Gold Standard for non-invasive tests for H. pylori Specificity 100% Sensitivity > 95%
H2N(13/14CO)NH2 + H20
Urease Enzyme
2NH3 + 13/14CO2

Page *

HeliCapTM
BreathCardTM
Urea Breath Test

Performance of Urea Breath Test

1. Swallow HeliCap™ with water. 2. After 10 min exhale into BreathCard™ until indicator changes colour. 3. Insert BreathCard™ in the Heliprobe® Analyzer and press Start (green button). 4. Result will be displayed after some minutes. Heliprobe 0 = patient not infectedHeliprobe 1 = borderline Heliprobe 2 = patient infected
*

Treatment
Incidence of ulcer relapse after 1 year
100 %
No eradication
Eradication
Eradication of Helicobacter pylori significantly reduces the recurrence of gastric ulcers
Treatment of gastric ulcer in H. pylori positive patients

Treatment and Eradication

Triple RegimenBismuth + Tetracycline + MetronidazoleClarithromycin + Amoxicillin + PPIQuadruple RegimenBismuth + Tetracycline + Metronidazole + PPILOAD (Levofloxaxin + Omeprazole + Nitazoxanide + Doxycycline)Sequential TherapyPPI + Amoxicillin (days 1-5) followed by PPI + Clarithromycin + Tinidazole (days 6 – 10)

Screening in low-incidence areas:symptomatic groups

4 . Premalignant lesions/conditions Chronic gastritis Gastric polyps Postgastrectomy Family history

Treatment of Gastric Cancer

Surgery Chemotherapy Radiotherapy

Surgery for gastric cancer

Billroth I and Billroth II resection

Billroth II resection

ADENOCARCINOMA OF THE STOMACH

Surgical resection only cure Late presentation makes sugary often futile Palliation controversial for Haemorrhage Gastric outlet Simple gastrectomy as effective as abdominal block Splenectomy often added due to direct involvement Only for the very distal partial gestrectomy Rest total gastrectomy Prognosis overall 12% 5 year survival 90% for stage I disease

Conclusion:

Although a multifactorial etiology , the main factors are infection with H. pylori The precancerous process is very prolonged, usually lasting several decades. Its intermediate steps are well-characterized histopathologically and may be reversible. A strategy of H. pylori screening and eradication will probably reduce gastric cancer incidence.

Other conditions

GASTRIC LYMPHOMA
5% of all primary gastric neoplasm's2 different types of lymphomaPart of systemic lymphoma with gastric involvement (32%)Part of primary involvement of the GIT (MALT Tumors)10 – 20% of all lymphomas occur in the abdomen50% of those are gastric in natureRisk factorsHP due to chronic stimulation of the MALT In early stages of disease Rx of HP leads to regression of the disease

GASTRIC LYMPHOMA Primary MALT

Treatment controversial Surgical treatment for patients without systemic involvement Mandatory for high grade lesions Possible not needed for low grade lesions Total gastrectomy and en-block for direct involvement Sparing duodenum and oesophagus Palliative resection with intra-abdominal spread Good for bleeding, obstruction and perforations Radiation and chemotherapy combination for most

GASTRIC SARCOMA

1 – 3 % of gastric malignanciesInclude a wide variety of tumorsLeiomyosarcomaLeiomyoblastomaGIST

Stomach and Duodenum 3